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Biomedical subjects

W Cheng

Publications and source records attributed to W Cheng.

At least 55 records · Page 3Linked to original sources
PubMed1999

Foreign-body ingestion in children: experience with 1,265 cases.

BACKGROUND/PURPOSE: This study aims to elucidate the clinical presentation, the effectiveness of investigations, and treatment of foreign body ingestion in children and to formulate an algorithm of management. METHODS: The records of children admitted to a single institution who had a history of foreign body ingestion over 33 years were reviewed. Symptoms, radiological findings, and endoscopic findings were assessed. RESULTS: Foreign bodies were detected in 552 (43%) of the 1,265 children admitted. The age of the children ranged from 6 months to 16 years (mean, 5.2 years). The preschool toddlers (mean age, 3.8 years) were most prone to ingest inanimate objects. The most common objects were coins (49%) and nonmetallic sharp objects (NMSO; 31%). Although x-rays could detect all the metallic objects and 86% of glass objects, the sensitivity of fish bone detection is only 26%. Absence of symptoms was common (50% in metallic group and 29% in NMSO group). Forty-one percent of coins and 95% of NMSO were lodged at sites suitable for removal by direct laryngoscopy alone with success rates of 86% and 77%, respectively. There were 3 disease-related complications and 1 mortality. Two of these children were mentally retarded and presented late. CONCLUSIONS: Efforts for prevention of ingestion of inanimate foreign body should focus on the preschool toddler group. Particular attention should be paid to mentally retarded children with vague gastrointestinal symptoms. Absence of symptoms does not preclude presence of foreign body in children. Children with history of NMSO ingestion should undergo direct laryngoscopy despite negative radiological finding, both as a screening procedure or treatment.

Child↗
PubMed1999

Residual bladder dysfunction 2 to 10 years after acute transverse myelitis.

OBJECTIVE: Acute transverse myelitis (ATM) is a relatively rare condition in children. The recovery rate is reported to be generally complete. In the current study, the long-term urological outcome of children with ATM was assessed. METHODOLOGY: The medical records of children with ATM admitted to Queen Mary Hospital, Hong Kong, over the last 15 years, were reviewed. RESULTS: The median age of the five children with ATM at the time of onset was 6 years (range = 2-12 years). The median length of follow up was 5 years (2-10 years). Four children recovered completely from paraparesis; two had no urinary symptoms with normal micturition. However, video-urodynamic studies 3 years after the acute onset revealed that four out of the five children, including one without any urinary symptom, suffered from residual bladder dysfunction - two from contractile neurogenic bladder and two from intermediate type of neurogenic bladder. CONCLUSION: Residual bladder dysfunction is common in children suffering from ATM despite improvement of paraparesis and apparent lack of urological symptoms. Long-term follow up of urological function in these patients is recommended.

Acute Disease↗
PubMed1999

Selenium-dependent cellular glutathione peroxidase protects mice against a pro-oxidant-induced oxidation of NADPH, NADH, lipids, and protein.

Since our prior work indicated that Se-dependent cellular glutathione peroxidase (GPX1) was necessary for protection against paraquat lethality, the present studies were to elucidate the biochemical mechanisms related to that protection. Four groups of mice [Se-deficient or -adequate GPX1 knockout and wild-type (WT)] were injected (i.p.) with 50 mg paraquat/kg body weight and tissues were collected 0, 0.5, 1, 2, 3, or 4 h after the injection. Whereas the ratios of NADPH/NADP and NADH/NAD in lung were reduced by 50-70% only 0.5 h after the injection in all groups, these two ratios in liver of the Se-adequate WT were significantly higher than those of the three GPX1 knockout or deficient groups 2-4 h after the injection. The paraquat-induced pulmonary lipid peroxidation and hepatic protein oxidation, measured as F(2)-isoprostanes and carbonyl contents, respectively, peaked at 1 h in these three groups. No such oxidative events were shown in any tissue of the Se-adequate WT throughout the time course. Whereas the F(2)-isoprostane formation was accelerated by both GPX1 knockout and Se deficiency in liver, it was not significantly elevated by the paraquat treatment in brain of any group. The paraquat injection also resulted in temporal changes in lung GPX activity and GPX1 protein in the Se-adequate WT, and significant reductions in lung total SOD activity in the GPX1 knockout or deficient groups. In conclusion, GPX1 plays a critical role in maintaining the redox status of mice under acute oxidative stress, and protects against paraquat-induced oxidative destruction of lipids and protein in vivo. These protections of GPX1 seem to be inducible and coordinated with those of other antioxidant enzymes.

Animals↗
PubMed1999

Characterization of a soluble ternary complex formed between human interferon-beta-1a and its receptor chains.

The extracellular portions of the chains that comprise the human type I interferon receptor, IFNAR1 and IFNAR2, have been expressed and purified as recombinant soluble His-tagged proteins, and their interactions with each other and with human interferon-beta-1a (IFN-beta-1a) were studied by gel filtration and by cross-linking. By gel filtration, no stable binary complexes between IFN-beta-1a and IFNAR1, or between IFNAR1 and IFNAR2 were detected. However, a stable binary complex formed between IFN-beta-1a and IFNAR2. Analysis of binary complex formation using various molar excesses of IFN-beta-1a and IFNAR2 indicated that the complex had a 1:1 stoichiometry, and reducing SDS-PAGE of the binary complex treated with the cross-linking reagent dissucinimidyl glutarate (DSG) indicated that the major cross-linked species had an apparent Mr consistent with the sum of its two individual components. Gel filtration of a mixture of IFNAR1 and the IFN-beta-1a/IFNAR2 complex indicated that the three proteins formed a stable ternary complex. Analysis of ternary complex formation using various molar excesses of IFNAR1 and the IFN-beta-1a/IFNAR2 complex indicated that the ternary complex had a 1:1:1 stoichiometry, and reducing SDS-PAGE of the ternary complex treated with DSG indicated that the major cross-linked species had an apparent Mr consistent with the sum of its three individual components. We conclude that the ternary complex forms by the sequential association of IFN-beta-1a with IFNAR2, followed by the association of IFNAR1 with the preformed binary complex. The ability to produce the IFN-beta-1a/IFNAR2 and IFN-beta-1a/IFNAR1/IFNAR2 complexes make them attractive candidates for X-ray crystallography studies aimed at determining the molecular interactions between IFN-beta-1a and its receptor.

Chromatography, Gel↗
PubMed1999

Two antiatherogenic effects of progesterone on human macrophages; inhibition of cholesteryl ester synthesis and block of its enhancement by glucocorticoids.

The effects of progesterone and estradiol on cholesteryl ester (CE) formation by monocyte-derived human macrophages were examined. Formation was assessed from incorporation of 14C-cholesterol during a 20-h incubation with hormone and from that of 3H-oleate (3 h) after hormone removal. Progesterone inhibited cholesterol into CE and decreased CE cellular levels. Inhibition: 1) was reversed by progesterone removal; 2) was independent of the progesterone receptor (not blocked by the receptor antagonist RU40555); and 3) exhibited specific structural requirements; 11alpha-OH-progesterone was inhibitory, whereas its stereoisomer 11beta-OH-progesterone was not. In contrast to progesterone, estradiol was ineffective. We had reported that dexamethasone enhanced CE accumulation by human macrophages (1). In this study, we describe similar effects of the endogenous steroid, cortisol, and of the most widely prescribed glucocorticoid, prednisolone. Both steroids increased CE formation from two folds, in the presence of cholesterol-liposomes, to five folds, in the presence of modified low-density lipoprotein. Progesterone (0.1-1 micromol/L), added during glucocorticoid treatment, blocked this increase. The progesterone block: 1) was duplicated by the steroid receptor inhibitor RU40555; 2) was not reversed by hormone removal; and 3) reflected inhibition of glucocorticoid-induced increases in messenger RNA for acyl-CoA-cholesterol:acyl transferase. Thus, progesterone exerted two effects on macrophages: it acutely inhibited CE formation, and it prevented glucocorticoid-induced increases in acyl-CoA-cholesterol-acyl transferase gene expression and CE synthesis.

Arteriosclerosis↗
PubMed1999

Video-assisted thoracoscopic surgery for patent ductus arteriosus in low birth weight neonates and infants.

BACKGROUND: Video-assisted thoracoscopic surgery (VATS) has been assuming an expanded role in the management of cardiothoracic disease. As instrumentation and experience increase, VATS is being applied to treat smaller patients. We report our experience with 34 low birth weight infants undergoing VATS interruption of patent ductus arteriosus (PDA). METHODS: VATS allows PDA interruption without the muscle cutting or rib spreading of a standard thoracotomy. Four small, 3-mm incisions are made along the line of a potential thoracotomy incision. Ports placed through these incisions admit endoscopic instruments, a camera, and a vascular clip applier. RESULTS: Median age at surgery was 15.5 days (range: 1-44 days). Median weight at surgery was 930 g (range: 575-2500 g). Twenty patients weighed <1 kg, and 13 weighed <750 g. All patients had congestive heart failure and had either failed indomethacin therapy or had contraindications to indomethacin. Median surgical time was 60 minutes (range: 31-171 minutes). Echocardiography documented elimination of ductal flow in all patients. Operative mortality was zero. Four patients (4/34 = 12%) required conversion to open thoracotomy: 1 because of difficult exposure, 1 because of pulmonary dysfunction and anasarca, 1 because of a large 1-cm duct, and 1 because of coagulopathy and poor pulmonary compliance. Two patients died before discharge: 1 patient (surgical weight: 605 g) died on postoperative day 2 because of intracranial hemorrhage, and 1 patient (surgical weight: 1725 g) died on postoperative day 88 because of multiple system organ failure. Follow-up has demonstrated no PDA murmur in any patient, but echocardiography revealed trace ductal flow in 2 patients. CONCLUSIONS: VATS offers a minimally traumatic, safe, and effective technique for PDA interruption in low birth weight neonates and infants.

Cardiac Surgical Procedures↗
PubMed1999

Differences in induction of p53, p21WAF1 and apoptosis in relation to cell cycle phase of MCF-7 cells treated with camptothecin.

The DNA topoisomerase I (topI) inhibitor camptothecin (CPT), stabilizes so-called cleavable complexes which consist of topI covalently attached to 3' OH ends of DNA nicks. Collisions between the progressing DNA replication forks (occurring in S phase cells) or between the transcription driven RNA polymerase molecules (occurring in G1, S and G2 cells) and these complexes convert the latter into secondary DNA lesions which are unrepairable and lethal to the cell. Changes induced by CPT in the level of the tumor suppressor p53, cyclin-dependent kinase inhibitor p21WAF1 and proapoptotic protein Bax (all detected immunocytochemically), were measured separately in the nucleus and cytoplasm of individual human breast carcinoma MCF-7 cells by laser scanning cytometry (LSC) in relation to cell cycle position and induction of apoptosis. The initial transient cell arrest at the G1 checkpoint seen at 8-16 h of treatment with 0.15 microM CPT was accompanied by the rapid accumulation of p53 (preventable by cycloheximide) in the nucleus; the rise (>20-fold) in p53 was maximal for S phase cells. The magnitude of the nuclear p53 increase induced by CPT, at maximum, was 2-fold higher than that induced by the proteasome inhibitor N-acetyl-Leu-Leu-norleucinal (LLnL). While the accumulation of p53 was seen in all phases of the cycle, only G1 cells responded by induction ( approximately 60-fold increase) of p21WAF1. Inhibition of DNA replication by aphidicolin prevented the accumulation of p53 in S and G2/M but had no effect on its induction in G1 cells. Perturbation of cell progression through S phase was seen between 24-72 h of treatment, and it coincided with induction of Bax and apoptosis (both maximal in S phase cells). Thus, the changes observed in S phase cells (nuclear accumulation of p53 preventable by aphidicolin, induction of Bax, apoptosis), triggered by the collisions of DNA replication forks with the CPT-induced lesions, were distinct from the changes in G1 (nuclear p53 accumulation unaffected by aphidicolin, induction of p21WAF1) presumably triggered by collisions of RNA polymerase with the CPT-lesions. Great heterogeneity in expression of p53 and p21WAF1 of the G1 cell population in response to CPT was observed, which may reflect the intercellular variability in the rate of transcription (i.e., frequencies of collisions of RNA polymerase with the lesions). Thus, differences in the transcriptional activity of G1 cells may play a role in their sensitivity to CPT and similar topI inhibitors.

Apoptosis↗
PubMed1999

[The effect of Xuezhikang on oxidation of low-density lipoproteins in vitro].

OBJECTIVE: To study the effect of Xuezhikang on oxidation of human low-density lipoprotein. METHODS: In vitro experiment was used to study the effect of Xuezhikang on the change of human low-density lipoprotein. Relative electrophoresis movement rate after oxidation of low-density lipoprotein mediated by addition of copper ion was observed. RESULTS: Oxidation of low-density lipoprotein mediated by copper ion was accelerated as the time of action prolonged and the process was accompanied by increased relative electrophoresis movement rate. Oxidation of low-density lipoprotein by copper ion was inhibited significantly in the presence of Xue zhikang as compared with absence of XuezhiKang at all time points. A greater reduction of reactive electrophoresis movement rate up to 33.5%, (P < 0.05) was noted. With increase of Xuezhikang concentration, the extent of reduction increased. CONCLUSION: It is shown that human low-density lipoprotein can be oxidized by mediation of copper ion and XuezhiKang may inhibit the extent of oxidation of low-density lipoprotein by copper ion.

Copper↗
PubMed1999

[Changes of placental nitric oxide synthase in patients with pregnancy induced hypertension].

The objective of this study was to determine whether the expression of placental endothelial nitric oxide synthase (eNOS) and/or inducible nitric oxide synthase (iNOS) are changed in pregnancy induced hypertension (PIH). The placentas of 32 patients with PIH and 32 normal pregnancies were studied by immunohistochemistry (Avidin-Biotin-Complex method). The results showed there were eNOS and iNOS antigens in placental tissues from PIH and normal pregnancy. They were all localized in placental villi and syncytiotrophoblast cells. The expression of placenta eNOS decreased significantly in patients with PIH as compared with that of normal pregnancy. The expression of placenta eNOS in mild PIH was higher than that of moderate or severe PIH (P < 0.025, P < 0.005, respectively). There was a negative correlation between blood pressure and the expression of eNOS in placenta (P < 0.0005). There was no significant difference between the expression of iNOS in placenta with PIH and that in normal pregnancy. Also, there was no significant difference of the expression of iNOS in placenta between the mild and moderate PIH, or the mild and severe PIH. Furthermore, there was no correlation between blood pressure and the expression of iNOS in placenta with PIH. It is concluded that the decrease of the expression of eNOS in placenta may be associated with the pathogenesis of PIH.

Adult↗
PubMed1998

Electron microscopy and x-ray diffraction studies of Lotus tetragonolobus A isolectin cross-linked with a divalent Lewisx oligosaccharide, an oncofetal antigen.

The interactions of lectins with multivalent carbohydrates often leads to the formation of highly ordered cross-linked lattices that are amenable to structural studies. A particularly well ordered, two-dimensional lattice is formed from fucose-specific isolectin A from Lotus tetragonolobus cross-linked with difucosyllacto-N-neohexaose, an oligosaccharide possessing the Lewisx determinant, which is an oncofetal antigen. A combination of electron microscopy, x-ray diffraction, simulation of electron micrographs, and molecular model building was used to determine the relative positions of the tetrameric lectin and bivalent carbohydrate within the lattice. X-ray diffraction from unoriented pellets was used to determine the lattice dimensions and analysis of electron micrographs was used to determine the lattice symmetry. Molecular models of the lattice were constructed based on the known structure of the jack bean lectin concanavalin A and the high degree of sequence homology between the two lectins. Using the symmetry and dimensions of the lattice and its appearance in filtered electron micrographs, molecular models were used to determine the orientation of the lectin in the lattice, and to define the range of lectin-oligosaccharide interactions consistent with the structural data. The present study provides the first description of a highly ordered, two-dimensional, cross-linked lattice between a tetravalent lectin and a bivalent carbohydrate.

Antigens, Neoplasm↗
PubMed1998

Isolation and characterization of an Enterococcus-like bacterium causing muscle necrosis and mortality in Macrobrachium rosenbergii in Taiwan.

A Gram-positive, ovoid, diplococoid bacterium tentatively identified as Enterococcus-like was isolated from diseased Macrobrachium rosenbergii in Taiwanese aquaculture ponds. The diseased prawns displayed poor growth, anorexia, inactivity, opaque and whitish musculature, and mortality. In histological preparations, melanized hemocytic granulomas were seen in the connective tissue around hemal sinuses together with hemocytic aggregation in necrotic musculature. Five isolates of diplococci were collected from diseased prawns at 4 farms and these were evaluated for 93 characteristics including morphology, physiology, biochemistry and sensitivity to antibiotics. The results indicated that the isolates belonged to a single species. They grew in 0.5 to 6.0% NaCl, at 10 to 40 degrees C, at pH 9.6 and on bile esculin medium, gave positive pyrrolidonylarylamidase, arginine dehydrolase and Voges-Proskauer tests, were resistant to bacitracin and SXT, and were CAMP-negative and non-hemolytic on sheep blood agar. These findings indicated an Enterococcus-like bacterium closely related to Enterococcus seriolicida (recently reduced to synonymy with Lactococcus garvieae). Experimental injection of 3 x 10(5) cells of strain KM002 of this Enterococcus-like bacterium into the ventral sinus of the prawn cephalothorax caused 100% mortality in 11 d, and induced muscular necrosis and hepatopancreatitis, gross signs and histopathology similar to those observed in the naturally infected prawns. It was concluded that this Enterococcus-like bacterium was the etiological agent associated with mortality of the farmed, diseased prawns.

Animals↗
PubMed1998

Enterococcus-like infections in Macrobrachium rosenbergii are exacerbated by high pH and temperature but reduced by low salinity.

Macrobrachium rosenbergii (10 to 15 g and 8 to 12 g at intermolt) were challenged with an enterococcus-like bacterium (strain KM002) previously isolated and identified as the causal agent of mortality. Challenge doses and conditions of pH, salinity and temperature were varied to determine the influence of environmental factors on the development of disease and mortality. Survival was 100% for the unchallenged control groups in all trials. In pH tests, the onset of mortality was earlier at pH 8.8 to 9.5 than at pH 4.6 to 5.2 and 7.5 to 7.7. Also, as pH 8.8 to 9.5, all challenged prawns died within 6 d in high dose challenge tests. By contrast, 20% of the prawns challenged at pH 4.6 to 5.2 and 7.5 to 7.7 survived. At low dose challenge (5 x 10(4) cfu prawn(-1)), survival increased significantly except at pH 8.8 to 9.5. In salinity tests at 2 challenge doses (1 x 10(6) and 2 x 10(7) cfu prawn(-1)), onset of mortality was earliest at 15 ppt and cumulative mortality was 100% at 15 ppt and 0 ppt. By contrast, survival was 80% at 5 and 10 ppt at the low dose challenge and 40% and 60%, respectively, at the high dose challenge. When the challenge dose was reduced to 5 x 10(4) cfu prawn(-1), survival was not significantly different at different salinity levels. In temperature tests at pH 7.2 to 7.5 and at 2 challenge doses (2 x 10(7) and 4 x 10(7) cfu prawn(-1)), the onset of mortality was earliest at 33 to 34 degrees C and total mortality occurred at 27 to 28 degrees C and 33 to 34 degrees C. By contrast, there were 40% and 20% survivors, respectively, for low and high challenge doses at 30 to 31 degrees C. Reducing the challenge dose to 5 x 10(4) cfu prawn(-1) gave higher survival in all groups. However, survival at 33 to 34 degrees C was still lowest. In similar temperature tests but at pH 8.8 to 9.5, onset of mortality was somewhat accelerated and there was 100% death for all the high challenge groups. At low challenge doses, mortality was lower but still highest in the 33 to 34 degrees C group. Results indicated that mortality of M. rosenbergii caused by this Enterococcus-like bacterium was exacerbated by environmental parameters of temperature and pH different from those known to be optimal for prawn growth. By contrast, low salinity appeared to have a beneficial effect on survival. Further work is needed to determine the mechanisms underlying these effects.

Animals↗
PubMed1998

Angiotensin II stimulation in vitro induces hypertrophy of normal and postinfarcted ventricular myocytes.

To determine whether angiotensin II (Ang II) stimulation of adult ventricular myocytes in vitro results in cellular hypertrophy, the changes in myocyte volume and protein content per cell were examined by confocal microscopy. Moreover, the possibility was considered that the upregulation of Ang II receptors on myocytes after infarction may potentiate and/or accelerate Ang II-mediated myocyte growth. Left ventricular myocytes isolated from control and failing hearts 3 days after infarction were cultured for 3 and 7 days in the presence of Ang II. Normal myocytes did not show an increase in volume and protein content at 3 days, but a 16% and 20% increase in these respective parameters was found at 7 days. Cell growth was faster and greater in myocytes from postinfarcted hearts. In these cells, myocyte volume increased 23% and protein content increased 28% at 3 days after Ang II administration. The higher hypertrophic reaction of myocytes from infarcted hearts occurred in spite of a 19% larger volume at isolation. In both groups of myocytes, the AT1 receptor blocker losartan completely inhibited the consequences of Ang II. Conversely, the AT2 receptor antagonist PD123319 had no effect on Ang II-induced hypertrophy. In conclusion, Ang II promotes myocyte growth through the activation of AT1 receptors, which modulate the time and magnitude of this cellular response.

Angiotensin II↗
PubMed1998

Identification of an allosteric binding site on the transcription factor p53 using a phage-displayed peptide library.

Monoclonal antibody PAb1620 recognizes a conformational epitope on the transcription factor p53 and, upon binding, allosterically inhibits p53 binding to DNA. A highly diverse (1.5 x 10(10) members) phage-displayed library of peptides containing 40 random amino acids was used to identify the PAb1620 binding site on p53. Panning this library against PAb1620 resulted in three unique peptides which have statistically significant sequence identities with p53 sufficient to identify the binding site as being composed of amino acids 106-113 and 146-156. Based on these results, we propose a mechanism by which PAb1620 can allosterically inhibit p53 binding to DNA through an indirect interaction between the antibody binding site and the L1 loop (amino acids 112-124) of p53, which is a component of the DNA binding region.

Allosteric Regulation↗
PubMed1998

Intracellular calcium, DNase activity and myocyte apoptosis in aging Fischer 344 rats.

Myocyte apoptosis increases with age in Fischer 344 rats, but the multiple molecular events implicated in this phenomenon remain to be identified. Several defects involving Ca2+ homeostasis, pH, and the expression of p53 and genes of the Bcl-2 protein family may contribute to the activation of myocyte death. Therefore, changes in intracellular pH, cytosolic Ca2+, DNase I and DNase II were measured in myocytes isolated by enzymatic digestion from rats of different ages. Moreover, the expression of p53, Bcl-2 and Bax in these cells was determined. Measurements of intracellular pH by BCECF fluorescence at 3, 12 and 24 months showed that this parameter did not change with age: 3 months, 7.20+/-0.05; 12 months, 7.21+/-0.07; 24 months, 7.18+/-0.09. In contrast, diastolic Ca2+ determined by the Fura 2-AM method increased progressively from 99.8+/-1.9 nm at 3 months to 136.3+/-9.6 nm at 24 months (P<0.001). Concurrently, DNase I activity evaluated by plasmid digestion assay in myocytes increased 3.2-fold from 3 to 24 months (P<0.02). Conversely, pH-dependent-DNase II remained essentially constant with age. Western blotting performed on ventricular myocytes did not detect significant changes in p53, Bax and Bcl-2 proteins with age. Similarly, immunocytochemically, the fraction of myocytes labeled by p53, Bax and Bcl-2 did not change from 3 to 24 months. In conclusion, myocyte aging is characterized by an increase in diastolic calcium which may activate DNase I triggering apoptosis, independently from the expression of p53, Bax and Bcl-2 in the cells.

Aging↗
PubMed1998

Investigating the dielectric effects of channel pore water on the electrostatic barriers of the permeation ion by the finite difference Poisson-Boltzmann method.

In this paper, the finite difference Poisson-Boltzmann (FDPB) method with four dielectric constants is developed to study the effect of dielectric saturation on the electrostatic barriers of the permeation ion. In this method, the inner shape of the channel pore is explicitly represented, and the fact that the dielectric constant inside the channel pore is different from that of bulk water is taken into account. A model channel system which is a righthanded twist bundle with four alpha-helical segments is provided for this study. From the FDPB calculations, it is found that the difference of the ionic electrostatic solvation energy for wider domains depends strongly on the pore radius in the vicinity of the ion when the pore dielectric constant is changed from 78 to 5. However, the electrostatic solvation energy of the permeation ion can not be significantly affected by the dielectric constant in regions with small pore radii. Our results indicate that the local electrostatic interactions inside the ion channel are of major importance for ion electrostatic solvation energies, and the effect of dielectric saturation on the electrostatic barriers is coupled to the interior channel dimensions.

Amino Acid Sequence↗
PubMed1998

Apoptosis and myocardial infarction.

Myocardial infarction was produced in rats and the contribution of apoptotic and necrotic myocyte cell death was measured quantitatively. Myocyte cell death by apoptosis involved 2.8 million cells at 2 hours after coronary artery occlusion and necrosis only 90,000 cells. Myocyte apoptosis continued to represent the major form of cell death, affecting 6.6 million cells at 4.5 hours, whereas myocyte necrosis peaked at 1 day, including 1.1 million cells. Apoptotic myocyte cell death was also present in the surviving portion of the wall adjacent to and remote from the infarcted myocardium where it peaked at 1-2 days. At this interval, 700/10(6) and 110/10(6) myocyte nuclei were undergoing apoptosis in the non-infarcted tissue bordering on and away from the ischemic area, respectively. Myocyte necrosis was absent in the viable myocardium after infarction. Since mechanical forces produced by pathologic loads may activate apoptosis, papillary muscles were exposed to high levels of resting tension in vitro and the magnitude of cell death in these samples was determined. Overstretching resulted in a 21-fold increase in apoptotic myocyte cell death which was coupled with the formation of reactive oxygen species, side-to-side slippage of myocytes, and depressed tension generation of the myocardium. In conclusion, apoptotic myocyte cell death plays a major role in ventricular remodeling after infarction, but whether physical forces, oxidant stress, architectural rearrangement of myocytes, and impaired force development of the myocardium in vivo are causaly related requires further investigation.

Animals↗